Modulation of NMDA-induced cytosolic calcium levels by ACPC in cultured cerebellar granule cells.

F X Sureda, E Viu, A Zapata, J L Capdevila, A Camins, E Escubedo, J Camarasa, R Trullas

Index: Neuroreport 7(11) , 1824-8, (1996)

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Abstract

The effect of 1-aminocyclopropanecarboxylic acid (ACPC) on the potentiation by glycine of N-methyl-D-aspartate (NMDA)-evoked increases in intracellular free calcium concentration [Ca2+]i was examined in cultured rat cerebellar granule cells. NMDA (50 microM) produced a rapid and sustained increase in [Ca2+]i from 72 +/- 3 to 205 +/- 18 nM. Addition of exogenous glycine potentiated (EC50 -2 microM) the effects of NMDA, increasing [Ca2+]i to an Emax of 323 +/- 5 nM. ACPC increased the EC50 of glycine from 2 microM (no ACPC) to 17 microM (400 microM ACPC). Concomitant with reduced potency of glycine, ACPC also inhibited the Emax of glycine to enhance NMDA-evoked cytosolic free calcium to values (224 +/- 1 nM) approaching those observed in the nominal absence of glycine. These results show that ACPC, a compound previously reported to prevent excitotoxic cell death, inhibits the glycine-induced increase of Ca2+ entry through NMDA receptors in cerebellar granule cells.